Development of vasomotor responses in fetal mesenteric arteries

Rouwet, Ellen V.; Mey, Jo G. R. De; Slaaf, Dick W.; Heineman, Erik; Ramsay, Graham; Noble, F.A.C. le

doi:10.1152/ajpheart.2000.279.3.h1097

Cited by 16 publications

(23 citation statements)

References 11 publications

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“…Images were projected onto a Hamamatsu camera attached to an intensifying unit. The camera was connected to a video recorder (Panasonic) and images were stored on S-VHS tape for off-line analysis of vessel dimensions, and blood flow characteristics (Rouwet et al, 2000).…”

Section: Time-lapse Video-microscopymentioning

confidence: 99%

Flow regulates arterial-venous differentiation in the chick embryo yolk sac

et al. 2004

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Formation of the yolk sac vascular system and its connection to the embryonic circulation is crucial for embryo survival in both mammals and birds. Most mice with mutations in genes involved in vascular development die because of a failure to establish this circulatory loop. Surprisingly,formation of yolk sac arteries and veins has not been well described in the recent literature. Using time-lapse video-microscopy, we have studied arterial-venous differentiation in the yolk sac of chick embryos. Immediately after the onset of perfusion, the yolk sac exhibits a posterior arterial and an anterior venous pole, which are connected to each other by cis-cis endothelial interactions. To form the paired and interlaced arterial-venous pattern characteristic of mature yolk sac vessels, small caliber vessels of the arterial domain are selectively disconnected from the growing arterial tree and subsequently reconnected to the venous system, implying that endothelial plasticity is needed to fashion normal growth of veins. Arterial-venous differentiation and patterning are controlled by hemodynamic forces, as shown by flow manipulation and in situ hybridization with arterial markers ephrinB2 and neuropilin 1, which show that expression of both mRNAs is not genetically determined but plastic and regulated by flow. In vivo application of ephrinB2 or EphB4 in the developing yolk sac failed to produce any morphological effects. By contrast, ephrinB2 and EphB4 application in the allantois of older embryos resulted in the rapid formation of arterial-venous shunts. In conclusion, we show that flow shapes the global patterning of the arterial tree and regulates the activation of the arterial markers ephrinB2 and neuropilin 1.

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Section: Time-lapse Video-microscopymentioning

confidence: 99%

Flow regulates arterial-venous differentiation in the chick embryo yolk sac

et al. 2004

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“…9 In short, the egg was opened, the chorioallantoic membrane was penetrated, and a segment of the intestine with its mesentery was exposed and stabilized. The egg was placed in a temperature-and air flow-controlled single-egg chamber (37°C, 4 L/min).…”

Section: Peripheral Arterial Controlmentioning

confidence: 99%

“…Administration of these drug concentrations to the mesentery has previously been shown to result in physiologically relevant vasomotor responses. 9 Functional autonomic nervous control of the peripheral vasculature was assessed by measurement of the arterial constrictor response to topically applied tyramine (20-L aliquots, 10 Ϫ6 to 10 Ϫ2 mol/L). Tyramine releases norepinephrine from perivascular sympathetic nerve endings without affecting presynaptic reuptake.…”

Section: Peripheral Arterial Controlmentioning

confidence: 99%

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Hypoxia Induces Aortic Hypertrophic Growth, Left Ventricular Dysfunction, and Sympathetic Hyperinnervation of Peripheral Arteries in the Chick Embryo

et al. 2002

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Background-Low birth weight is associated with an increased incidence of cardiovascular diseases, including hypertension, later in life. This suggests that antenatal insults program for fetal adaptations of the circulatory system. In the present study, we evaluated the effects of mild hypoxia on cardiac function, blood pressure control, and arterial structure and function in near-term chick embryos. Methods and Results-Chick embryos were incubated under normoxic (21% O 2 ) or hypoxic (15% O 2 ) conditions and evaluated at incubation day 19 by use of histological techniques, isolated heart preparations, and in vivo measurements of sympathetic arterial tone and systemic hemodynamics. Chronic hypoxia caused a 33% increase in mortality and an 11% reduction in body weight in surviving embryos. The lumen of the ascending aorta in hypoxic embryos was 23% smaller. Left ventricular systolic pressure was 22% lower, and heart weight/body weight ratio was 14% higher. In resistance arteries of hypoxic embryos, in vivo baseline tone was 23% higher, norepinephrine sensitivity was similar, and norepinephrine release from sympathetic nerves increased 2-fold, indicating sympathetic hyperinnervation. Mean arterial pressure and heart rate were similar under resting conditions, but chronically hypoxic embryos failed to maintain blood pressure during acute stress. Conclusions-This study indicates that mild hypoxia during embryonic development induces alterations in cardiac and vascular function and structure and affects hemodynamic regulation. These findings reveal that antenatal insults have profound effects on the control and design of the circulatory system that are already established at birth and may program for hypertension and heart failure at a later age.

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“…During acute hypoxia, NE levels rise from 0.1 M up to 0.8 M in the chicken embryo (24). ␣ 1 -Adrenergic stimulation in response to acute hypoxia resulting in peripheral vasoconstriction has directly and indirectly been shown in the intact chicken embryo (25,31). In the intact embryo, the arterial system may not only be exposed to vasoconstrictors such as NE, but also to a tonic endothelial dilator influence.…”

Section: Relevance For In Vivo Hemodynamics During Acute Hypoxemiamentioning

confidence: 99%

Direct effects of acute hypoxia on the reactivity of peripheral arteries of the chicken embryo

Ruijtenbeek

Kessels

Villamor

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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. Direct effects of acute hypoxia on the reactivity of peripheral arteries of the chicken embryo. Am J Physiol Regulatory Integrative Comp Physiol 283: R331-R338, 2002. First published April 4, 2002 10.1152/ajpregu.00675.2001.-In the chicken embryo, acute hypoxemia results in cardiovascular responses, including an increased peripheral resistance. We investigated whether local direct effects of decreased oxygen tension might participate in the arterial response to hypoxemia in the chicken embryo. Femoral arteries of chicken embryos were isolated at 0.9 of incubation time, and the effects of acute hypoxia on contraction and relaxation were determined in vitro. While hypoxia reduced contraction induced by high K ϩ to a small extent (Ϫ21.8 Ϯ 5.7%), contractile responses to exogenous norepinephrine (NE) were markedly reduced (Ϫ51.1 Ϯ 3.2%) in 80% of the arterial segments. This effect of hypoxia was not altered by removal of the endothelium, inhibition of NO synthase or cyclooxygenase, or by depolarization plus Ca 2ϩ channel blockade. When arteries were simultaneously exposed to NE and ACh, hypoxia resulted in contraction (ϩ49.8 Ϯ 9.3%). Also, relaxing responses to ACh were abolished during acute hypoxia, while the vessels became more sensitive to the relaxing effect of the NO donor sodium nitroprusside (pD2: 5.81 Ϯ 0.21 vs. 5.31 Ϯ 0.27). Thus, in chicken embryo femoral arteries, acute hypoxia blunts agonist-induced contraction of the smooth muscle and inhibits stimulated endothelium-derived relaxation factor release. The consequences of this for in vivo fetal hemodynamics during acute hypoxemia depend on the balance between vasomotor influences of circulating catecholamines and those of the endothelium.catecholamine; endothelium-derived relaxation factor IN THE FETUS, AN ACUTE DECREASE in arterial oxygen tension leads to cardiovascular responses, involving an elevation in blood pressure and redistribution of the cardiac output in favor of vital organs. In fetal lambs (10), fetal llamas (9), and chicken embryos (24, 25), increased levels of circulating catecholamines take part in this response. Early in gestation, the chromaffin cells in the primitive adrenal medulla are directly sensitive to low oxygen tension. Later in gestation, activation of efferent sympathetic nerves also contributes to the response (38). Antagonists of ␣-adrenoreceptors blunt the hypoxia-induced increase in fetal total peripheral resistance (9, 10, 25).Neurohumoral mechanisms have been proposed to be important regulators of blood flow in the hypoxemic fetus, but it remains to be established whether local and direct effects of decreased oxygen tension participate in the fetal cardiovascular response to hypoxemia. In previous studies, we have shown that chronic exposure to hypoxia affects both sympathetic innervation (34) and endothelium-dependent relaxation (33) of femoral arteries of the chicken embryo, but acute effects of hypoxia in isolated systemic arteries were not studied. Moreover, acute effects of low oxygen tension have been studied i...

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Development of vasomotor responses in fetal mesenteric arteries

Cited by 16 publications

References 11 publications

Flow regulates arterial-venous differentiation in the chick embryo yolk sac

Flow regulates arterial-venous differentiation in the chick embryo yolk sac

Hypoxia Induces Aortic Hypertrophic Growth, Left Ventricular Dysfunction, and Sympathetic Hyperinnervation of Peripheral Arteries in the Chick Embryo

Direct effects of acute hypoxia on the reactivity of peripheral arteries of the chicken embryo

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